Genetic factors contribute significantly to the individual differences in the response to painful stimuli with upwards of 60% of these differences attributed to genetic variation. The focus of my lab is to identify the individual gene candidates and the families of genes that contribute to differences in pain responses. Using genomewide methodologies for the identification of novel candidate genes along with targeted testing of specific genes and their associated pathways, I have been able to successfully explore the genetic contribution to both somatic and visceral pain behaviors. To this end, my recent work has focused on identifying genetic contributions to abdominal pain susceptibility in preclinical and clinical models of Irritable Bowel Syndrome, a functional abomdinal pain disorder characterized by pain in the absence of bowel pathology or damage. My research encompasses the entire translational science spectrum from animal models to molecular analyses and then all the way to the patient populations of interest. The candidate genes identified in preclinical models can then be examined in clinical populations to determine whether these genes contribute to pain susceptibility in patients and shed light on novel targets for therapeutic intervention designed to address pain at the source.